DIABETES MELLITUS AND PITUITARY DISORDERS  NO insulin production Prone for DKA

Management:

 Diet
 Exercise
 Insulin

Type II (NIDDM)

 Maturity – onset, Stable DM, Ketosis – resistant

DM
 Onset is 40 years
 Common in obese adults
 Inadequate insulin production or cells do not
respond to insulin
 Prone for HHNKS
Diabetes Mellitus
Management:
 a chronic metabolic disease characterized by
hyperglycemia due to disorder of carbohydrate,  Diet
fat and protein metabolism  Exercise
 OHA, Insulin in STRESSFUL situation
Predisposing Factors:
Hyperglycemia  Polyuria, Polydipsia, Polyphagia
 Heredity: strongly associated with Type II DM
 Obesity: Adipose tissues are resistant to insulin, Pathophysiology
therefore glucose uptake by the cells is poor Hyperglycemia
 Stress: Stimulates secretion of epinephrine, nor- ↓
epinephrine, glucocorticoids  increased serum Large amounts of glucose pass thru kidneys
carbohydrates ↓
 Viral infection: increase risk to autoimmune It will exert high osmotic pressure w/in the renal
disorders tubules
 Autoimmune Disorders: more associated with ↓
Type I DM Osmotic diuresis
 Multigravida Women: with large babies ↓
Polyuria
Types of DM

 Type I
 Type II
 Gestational Diabetes
 Diabetes associated with other conditions or
syndromes
o Pancreatic disease, Cushing’s syndrome
o Use of certain drugs
 Due to blood osmolarity, water moves from
o Steroids
inside to outside the cell (ICF dehydration)
Type I (IDDM)  There will be hypovolemia (ECF dehydration)
 Glycosuria will occur if glucose in the blood is
 Juvenile – onset, Brittle DM, Unstable DM
>220mg/dl (renal threshold)
 Onset is less than 30 years
 Common in children or in non-obese adults Glucose Insulin Cell
↓
 Cellular o Infections, Periodontal, UTI, Vasculitis,
Starvation Cellulitis, Vaginitis, Furuncles,
↓ Carbuncles, Retarded Wound Healing
Hunger & ↑Appetite  Polyphagia
Complications:

Glucose Cell  Macroangiopathy

o Brain: Cerebrovascular accident
Cellular o Heart: Myocardial infarction
Starvation o Peripheral arteries: peripheral vascular
Protein disease
Fats Ketones  Microangiopathy
Polyphagia o Kidneys: renal failure due to
nephropathy
o Eyes: cataracts due to retinopathy
 Neuropathy
o Spinal Cord/ ANS
o Peripheral neuropathy
 involves damage to the PNS
 affect movement, sensation and
bodily functions (numbness/
tingling)
o Paralysis
o Gastroparesis (delayed gastric
emptying)
o Neurogenic bladder (bladder does not
o empty properly)
o Decreased Libido, impotence
 Ketones act as CNS depressants and may
decrease brain pH leading to coma Diagnostic Test

 Random Blood Sugar (RBS)

o Blood specimen is drawn without
preplanning
o ≥200mg/dl + symptoms is suggestive of
DM
 Fasting Blood Sugar (FBS)
o Blood specimen after 8 hours of fasting
o No DM (70-110 mg/dl)
 Postprandial Blood Sugar
o Blood sample is taken 2 hrs after a high
CHO meal
o No DM (70-110mg/dl), DM (≥140)
 Oral Glucose Tolerance Test (OGTT)
o Client then fast for 8 hours. A baseline
blood sample is drawn & a urine
specimen is collected
 Due to increased blood viscosity o An oral glucose solution is given
o Sluggish circulation
o Proliferation of microorganisms
 o Blood is drawn at 30 minutes & 1, 2, Intermediate
and 3 hours after the ingestion of - NPH 1-2 hrs 6-12 hrs 18-24 hrs
glucose solution. Urine is collected - Humulin N 1-2 hrs 8-12 hrs 18-24 hrs
o No DM (glucose returns to normal in 2- - Lente, Humulin L 1-2 hrs 8-12 hrs 12-28 hrs
3 hours & urine is negative for glucose) Long acting
o DM (blood glucose returns to normal - Ultralente 5-8 hrs 14-20 hrs 30-36 hrs
- Lantus UK UK 24 hrs
slowly; urine is positive for glucose)
 Glycosylated hemoglobin (HbA1c)
o The amount of glucose stored by the Nursing Responsibilities
hemoglobin is elevated above 7% in the
Insulin Therapy:
newly diagnosed client with DM, in one
who is noncompliant, or in one who is  Route: SubQ
Inadequately treated o slow absorption, less painful, 90° (thin)
45° obese clients,
Management
o no need to aspirate, do not massage
 Diet site of injection
o Low caloric diet specially if obese o IV insulin: given in emergency cases
o Diet should be in proportion (DKA)
 20% CHON  Administer insulin at room temperature
 30% Fats o Cold insulin can cause lipodystrophy
 50% CHO
Lipoatrophy - loss of subcutaneous fat usually caused by
o Consume complex CHO and HIGH fiber
the utilization of animal insulin
diet
 inhibits glucose absorption in Lipohypertrophy - development of fibrofatty masses,
the intestines usually caused by repeated use of injection site
 Exercise
o Increases CHO uptake by the cells  Store vial of insulin in current use at RT
o Decreases insulin requirements o Insulin can be stored at RT for 1 month
o Maintains ideal body weight, serum o Other vials should be refrigerated
carbohydrates & serum lipids  Rotate the site of injection
 Medications: o To prevent lipodystrophy
o Insulin (for type I and type II) o Lipodystrophy inhibits insulin
o Oral Hypoglycemic Agents (OHA) absorption
For type I  Gently roll vial in between the palms to
 Sulfonylureas redistribute insulin particles
 Nonsufonylureas  DO NOT Shake
- Biguanides o bubbles make it difficult to aspirate
- Alpha-glucosidase inhibitors exact amount
- Thiazolidinediones  Observe for side effects of insulin therapy
- Meglitinides o Localized: Induration or Redness,
Swelling, Lesion at the site,
Insulin Onset Peak Duration Lipodystrophy
Rapid Acting o Generalized:
- Lispro (Humalog) 5 mins 30 mins-1 2-4 hours  Edema: due to sudden
- Aspart (Novalog) hr
resolution of hyperglycemia
Short Acting
 Hypoglycemia
- Regular (Humulin 30 min – 2 – 4 hrs 6-8 hrs
 Somogyi phenomenon
R, Novolin R, Iletin 1 hr
II regular)  Sulfonylureas “insulin releasers”
 o Stimulate the beta cells to secrete more o 3-4 oz regular soft-drink, 8 oz fruit
insulin juice, 5-7 pcs lifesaver’s candies, 3-4
o Increases the ability of insulin cell pcs hard candies, 1 tblsp sugar, 5 ml
receptors to bind insulin pure honey/ karo syrup
o SE: weight gain, hypoglycemia, o 10-15 gm CHO
secondary failure of pancreas due to o D5W 20-50 ml IV push ( if unconscious)
overstimulation or 1 mg glucagon
 Tolbutamide (Orinase) o Monitor BS (blood sugar)
 Acetohexamide (Dymelor)
Diabetes Ketoacidosis (DKA)
 Tolazamide (Tolinase)
 Chlorpropamide (Diabenese)  Acute complication of DM characterized by
 Glipizide (Glucotrol) o Hyperglycemia
 Glyburide (micronase, Glynase) o accumulation of ketones in the body;
 Glimepiride (Amaryl) causes metabolic acidosis
 Nonsulfonylureas o frequently occurs in DM Type I (IDDM)
o Biguanides
 Metformin (Glucophage) Precipitating factors:
 Help tissues use available
 undiagnosed diabetes
insulin more efficiently
 neglect of treatment
 “insulin sensitizers”
 infection, cardiovascular disorder
 SE: Stomach upset, flatulence,
 other physical or emotional stress
diarrhea
 no weight gain, no Assessment
hypoglycemia unlike
sulfonylureas  3 P’s
o Alpha-glucosidase inhibitors  N&V, abdominal pain
 Miglitol (Glyset), Acarbose  warm, dry, flushed skin
(Precose)  dry mucous membranes; soft eyeballs
 Alpha-glucosidase is an  Kussmaul’s respirations or tachypnea; acetone
intestinal enzyme that breaks breath or fruity breath
down carbohydrates into  Altered LOC
glucose, when this enzyme is  Hypotension
inhibited, the process of  Tachycardia
forming glucose is slowed and Diagnostic Test
glucose is absorbed more
slowly from the small intestine  Serum glucose (up to 600 mg/dL) and ketones
 Taken 15 minutes before meal elevated (positive urine ketones)
 BUN, Creatinine, Hematocrit are elevated (due
Hypoglycemia
to dehydration)
Causes:  Serum sodium decreased, potassium (elevated
due to the acidosis)
 Overdose of insulin, omission of meals,  ABGs: metabolic acidosis with compensatory
Strenuous exercise, G.I. upset (N&V) respiratory alkalosis
Assessment: Nursing Management
 <60 mg/dl  Maintain a patent airway.
Management  Maintain F&E balance.
o Administer IV therapy as ordered.
 Simple Sugars p.o.
  Normal saline (0.9% NaCl), then  Urine positive for glucose
hypotonic (0.45% NaCl) sodium
chloride
o When blood sugar drops to 250 mg/dl, Nursing interventions:
may add 5% dextrose to IV
o Potassium will be added when the urine  treatment and nursing care is similar to DKA,
output is adequate. excluding measures to treat ketosis and
metabolic acidosis
 Observe for fluid and electrolyte imbalances,
especially fluid overload, hypokalemia &
hyperkalemia
 Administer insulin as ordered.
o ONLY Regular insulin is given IV (drip or
push) and/or subcutaneously (SC).
o If given IV drip, give with small amounts
of albumin since insulin adheres to IV
tubing
o Monitor blood glucose levels frequently.
 Check urine output every hour
 Monitor vital signs
 Assist client with self-care
 Provide care for the unconscious client if in a
coma
 Discuss with client the reasons ketosis
developed and provide additional diabetic
teaching if indicated

Hyperosmolar Hyperglycemic Nonketotic Syndrome

(HHNKS)

 A complication of DM characterized by
o Hyperglycemia
o Hyperosmolar state without ketosis
 Occurs in Type II DM
 Precipitating factors are:
o undiagnosed diabetes
o Infections, major burns, other stress
o certain medications (Dilantin, Thiazide
diuretics)
o Dialysis, Hyper-alimentation, pancreatic
disease

Assessment findings:

 Similar to ketoacidosis but without Kussmaul

respirations and acetone breath

Laboratory tests

 Blood glucose level extremely elevated

 BUN, creatinine, Hct elevated (due to
dehydration)